Muscle Energy Technique (MET) with variant and techniques.
Endo – Perio lesions.ppt
1. Endo – Perio lesions:
An enigma to the clinician?
Dr. Nikhat Fatima
Rama Dental College, Hospital
Research center
2. • It’s the spread of inflammation and
infection from one component to the
other.
First described by Simring and Goldberg in 1964
3. Pulpal and Periodontal problems are responsible
for more than 50% of tooth mortality.
Chen SY,Wang HI,Clickman GN. The influence of
endodontic treatment upon periodontal wound
healing. J Clin periodontal24;449-456,1997
Bender IB. Factors influencing radiographic
appearance of bony lesions. J Endod 8;161-
170,1982
4. • The periodontium and the pulp have
embryonic, anatomic and functional
interrelationship.
• They are ectomesenchymal in origin,
from which the cells proliferate to
form the dental papilla and follicle,
which are the precursors of the pulp
and the periodontium respectively.
6. • Pathways are developed that provide
means by which pathological agents pass
between the pulp and the periodontium,
thereby creating the perio – endo lesion.
7. • Three main avenues for communication
are,
• 1) Dentinal tubules.
• 2) Lateral and accessory canals and
• 3) The apical foramen
“The endo-perio lesion: a critical appraisal
of the disease condition”
ILAN ROTSTEIN & JAMES H. SIMON
12. • These inflammatory lesions
cause localized oedema and
a resulting increase in intra-
pulpal pressure and cell
death.
13. Bacteria Associated with Periodontitis
Very strong Strong Moderate
A actinomyecetemcomitans P intermedia S intermedius
P gingivalis C rectus P micros
B forsythus E nodatum F nucleatum
Treponema sp E corrodens
Eubacterium sp
14. Pathogenesis
• Periodontal lesions are initiated by
deposits of plaque and calculus:
• The toxins produced by these
bacteria can irritate the gum tissues
and cause the body’s immune
system to “turn on” (chronic
inflammation) – this inflammation
can break down and destroy the
tissues and bone supporting the
tooth.
• The gum tissues separate from the
tooth, forming pockets. As the
disease progresses, the pockets
deepen, destroying more supporting
tissues.
15.
16. Classification (Simon 1972)
• Based on the primary source of
infection
• PRIMARY ENDODONTIC LESION.
• Chronic apical lesion on a tooth with a
necrotic pulp may drain coronally
through the periodontal ligament into
the gingival sulcus.
• Usually heals following root canal
treatment.
17. • These lesions are caused
primarily by periodontal
pathogens. In this process,
chronic periodontitis progresses
apically along the root surface. In
most cases, pulpal tests indicate
a clinically normal pulpal
reaction. There is frequently an
accumulation of plaque and
calculus and the pockets are
deep.
PRIMARY PERIODONTIC LESION
18. Primary endodontic lesion with secondary
periodontal involvement
• If it is untreated primary endodontic
lesion involves with secondary
periodontal breakdown.
• This may also occurs as a result of
root perforation during root canal
treatment, or where pins and posts may
have been misplaced during restoration
of the crown. Root fractures may also
be present.
19. Primary periodontal disease with secondary
endodontic involvement
• The apical progression of a
periodontal pocket may continue
until the apical tissues are involved.
• In this case, the pulp may become
necrotic as a result of infection
entering via lateral canals or the
apical foramen.
20. True combined lesions
• Occurs less frequently than others. It is
formed when an endodontic lesion
progressing coronally joins an infected
periodontal pocket progressing
apically.
• In molar teeth, root resection can be an
alternative treatment.
• The prognosis of a true-combined
perio-endo lesion is often poor or even
hopeless, especially when periodontal
lesions are chronic with extensive loss
of attachment.
22. Diagnosis
• Pain
• Swelling
• Mobility
• Suppuration
• Periodontal probing
• Presence of local deposits
• Presence of caries and restoration
• Palpation
• Pulp vitality test
• Radiographic interpretation
23. Periodontal Abscesses
A localized purulent infection
that involves the marginal
gingiva or interdental papilla.
Clinical Features
– Smooth, shiny swelling of the
gingiva
– Painful, tender to palpation
– Purulent exudate
– Increased probing depth
– Mobile, percussion sensitive
– Tooth usually vital
24. • This fistula on the labial
surface looks like an
endodontic abscess.
• Diagnosis of any abscess
must include periodontal
probing, periapical
radiographs ,vitality tests and
a patient history .
25. This case shows a
combination of periodontitis
and endodontic
inflammation
causing bone loss at the
crest and at the apex.
26. • As long as the pulp remains
vital, it is unlikely that
significant changes will occur
in the periodontium.
• The ability of inflammatory
periodontal disease to affect
the pulp is much less certain.
27. Clinical findings in endodontic
and periodontic lesions
CLINICAL FINDINGS ENDO LESION PERIO LESION
PULPAL RESPONSE ABSENT PRESENT
BONE DEFORMITY TUBULAR ‘U’ TRIANGULAR ‘V’
PLAQUE & CALCULUS ABSENT PRESENT
CARIES/ RESTORATION PRESENT ABSENT
MOBILITY ABSENT PRESENT
GEN PERIODONTITIS
ABSENT PRESENT
28. Clinical findings in endodontic and
combined endodontic-periodontic lesions
Clinical findings Endo lesion Combined lesion
Pulpal status Necrotic Necrotic
Perio status Normal Gen periodontitis
Probing Narrow pocket Wide pocket
Plaque and
calculus
Absent Present
Treatment Endodontic Combined
Prognosis Good Depends on perio
34. • In combined endodontic-periodontic
lesions, it is generally wise to treat
the Endodontic component first,
because in many cases this will lead
to complete resolution of the
problem.
35. • The location, extension, severity of
inflammation and the degree of
tissue involvement helps the dentist
to select the proper treatment.
36. Conclusion
• The clinical course of the disease
involving the pulpo- periodontal
complex is dictated by the bacterial
aetiology and thereby the treatment
plan is decided.
• Other factors such as patient co-
operation, restorability and economics
will influence the treatment decisions.
However the primary goal of all
treatment efforts must be to rid the
patient of the infection.
